The rhythmic closing of heart valves produces the distinct “lub-dub” sounds that characterize a heartbeat, formally known as the first (S1) and second (S2) heart sounds. The second sound, or “dub,” consists of two separate, rapid sounds: the closure of the aortic valve (A2) and the closure of the pulmonic valve (P2). A2 consistently precedes P2, meaning the aortic valve always closes slightly before the pulmonic valve. This difference in timing, known as “splitting” of the second heart sound, is a normal physiological phenomenon. This consistent timing difference is dictated by the vastly different pressure environments of the heart’s two sides, which determines when each valve is forced shut.
Understanding the Heart’s Two Sides
The human heart functions as two pumps operating side-by-side, each dedicated to a distinct circulatory system. The left side, including the left atrium and ventricle, handles systemic circulation, pushing oxygenated blood out to the entire body. The right side, with the right atrium and ventricle, manages pulmonary circulation, pumping deoxygenated blood only to the lungs.
These two systems operate against vastly different levels of resistance, which is the opposition to blood flow. Systemic circulation is a high-resistance, high-pressure system because it must overcome the friction and distance of all the body’s blood vessels. Pulmonary circulation is a low-resistance, low-pressure system because the lungs are close to the heart. This difference in workload is reflected in the muscular thickness of the ventricles, with the left ventricular wall being significantly thicker and more powerful than the right.
The Primary Cause of Valve Timing Differences
The distinct pressures in the two circulatory systems are the primary factor forcing the aortic valve to close before the pulmonic valve. Valve closure is a passive event, occurring when the pressure in the artery (aorta or pulmonary artery) exceeds the pressure in the relaxing ventricle below it, forcing the valve shut. The left ventricle must generate a high peak pressure, often around 120 millimeters of mercury (mmHg), to overcome the high resistance of systemic circulation.
Once the left ventricle begins to relax, its pressure falls rapidly due to the high pressure maintained in the aorta, typically 80 mmHg during relaxation. This large pressure gradient quickly reverses blood flow, slamming the aortic valve shut and producing the A2 sound. In contrast, the right ventricle only needs to generate a peak pressure of about 25 mmHg to pump blood into the low-resistance pulmonary artery.
Because the pressure gradient between the right ventricle and the pulmonary artery is much smaller, the right ventricle takes slightly longer to complete its ejection phase. The right ventricle’s lower peak pressure and the lower arterial pressure mean it takes more time for the ventricular pressure to drop below the arterial pressure required for closure. This slight prolongation of the right ventricular ejection time delays the closure of the pulmonic valve (P2), resulting in the characteristic A2-P2 timing sequence.
How Breathing Affects Valve Closure
While the pressure difference dictates the baseline timing, breathing introduces a dynamic variation known as physiological splitting. During inspiration, the chest cavity expands, creating a more negative pressure inside the chest. This negative pressure increases the flow of blood from the body’s veins into the right atrium and ventricle, a process called increased venous return.
The increased blood volume means the right ventricle has more to pump, which prolongs its ejection time and further delays the P2 sound. Simultaneously, the expanded lungs briefly hold more blood, slightly reducing the volume returning to the left side. This temporary reduction allows the left ventricle to complete its ejection sooner, causing A2 to close slightly earlier. The combined effect of a delayed P2 and an earlier A2 widens the A2-P2 interval during deep inspiration.
When a person exhales, the intrathoracic pressure returns to its pre-inspiration state, and the blood flow volumes normalize. The right ventricle’s filling volume decreases, which shortens its ejection time, causing P2 to move closer to A2. During expiration, the two valve closure sounds often merge so closely that they are heard as a single “dub” sound, which is the normal physiological state. This respiratory variation is a predictable and healthy response to changes in blood volume dynamics.
Why This Timing Matters to Doctors
The splitting of the second heart sound is an important diagnostic tool. Observing how A2 and P2 separate and merge with breathing can indicate the health of the heart’s electrical and mechanical function. Normal, or physiological, splitting is defined by the widening of the split during inspiration and its disappearance during expiration.
Abnormal patterns of splitting can point to underlying heart conditions. A fixed split occurs when the A2-P2 interval remains wide and does not change with respiration, often a sign of an atrial septal defect (a hole between the upper chambers of the heart). A paradoxical split is an inverted pattern where the split is heard on expiration but disappears on inspiration, suggesting a delay in left ventricular emptying, such as from severe aortic stenosis or a left bundle branch block. This predictable valve timing provides a non-invasive, initial clue to the mechanical efficiency of the heart’s two sides.